Adrian Tase
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LDL-C, HDL-C, statins, PCSK9-i’s, CETP-i’s.
Lipid-lowering drugs reached a peak since large scale development of statins, which control well LDL-Cand HDL-C levels.Beyond this “state-of-the-pharma”, recentresearch show that three are more efficient solutions. The dual clinical cases display distinct dyscolesterolaemic particularities which ask for innovative therapeutic solutions.The first clinical case is a 24 y. o. biomedical student, with severe coronary family history (a brother suddenly dead at the age of 28 y. o., father dead at 44 y. o. after the second MI), perfect preventive lifestyle, LDL-C 232 mg/dL, HDL-C 36 mg/dLandhs-CRP 3,6 mg/L. It was initiated a treatment with a redutable statin, in progressive dosages till the maximum one in the guidelines, LDL-C lowering to 202 mg/dL. Beyond statins, we can lower LDL-C more using PUFA and PCSK9 inhibitors.The second clinical case was a71 y. o. diabetic controlled by oral antidiabetics, with controlled hypertensionby ACE-inhibitors, LDL-C 65 mg/dL under statin. The subject presents with substernal pressure and emesis; an HDL-C value of 22 mg/mL and two tight stenoseson ACD segm. 1, and ADA segm. 2 are remarkable. Case interpretation: qualitative dimension – lowering HDL-C antioxidant capacity in acute coronary syndromes; quantitative dimension – low HDL-C remains a cardiovascular risk prediction in statin treated subjects. Beyond statins, we can increase more HDL-C using dalcetrapib, a CETP inhibitor. The drug classes proposed for these two patients are important pharmacologic tools in synergistic control of cholesterol fractions.
